Inflammation may occur in the eye following ocular surgery. Steroidal and nonsteroidal antiinflammatory agents (NSAIAs) have been used to relieve the inflammation. However, steroidal agents can induce an increase in intraocular pressure (Polansky et al., "Antiinflammatory Agents", in Sears, ed., Handbook of Experimental Pharmacology, Springer-Verlag, (1985), 69:459-538). The NSAIAs, such as salicylates, phenylbutazone, indomethacin, ibuprofen and naproxen, can produce numerous side effects, including edema, nausea, stomatitis, epigastric pain, peptic ulcer, agranulocytosis, hepatitis and drug rash. In addition, the NSAIAs may actually worsen the inflammation, especially during the late phase of the inflammation. This is because the clinically available NSAIAs at this time are primary cyclooxygenase inhibitors. Blocking the cyclooxygenase arm of the arachidonic acid (AA) cascade potentiates the production of lipooxygenase metabolites which are ultimately the leukotrienes (LT). LTs are responsible for the late phase of inflammation and for the chemotaxis of leukocytes (Miyano et al., Ophthalmic Res. (1984) 16:256-263; Chiou et al., J. Ocular Pharmacology (1985) 1:383-389; Bhattercherjee et al., "Effects of lipooxygenase products on leukocyte accumulation in the rabbit eye" in Samuelsson et al., eds., Leukotrienes and Other Lipoxygenase Products, Raven Press (1982) 325-330.) A previous study indicated that a new synthetic lipooxygenase inhibitor, REV 5901, was effective in reducing the late phase of inflammation. However, when REV 5901 was used alone in treatment of lens protein induced ocular inflammation, there was an increase in the early phase of inflammation. This observation was attributed to an increase in the production of prostaglandins caused by the inhibition of the lipooxygenase arm of the AA cascade. (Chang et al., J. Ocular Pharmacology, (1989) 5:353-360). The early phase of the inflammation has been effectively suppressed by indomethacin.